A new weight-loss pill

In the interest of Biochemisty I sat through an infomercial about a new weight-loss pill: Satise. This pill claims to contains a protein derived from a potato which promotes satiety (hence the name) thus affecting weight loss.

The infomercial mentioned cholecystokinin (rather quickly).

Cholecystokinin is normally secreted from the small intestines in the presence of partially digested fats and proteins. This in turns stimulates the pancreas and gallbladder to deliver digestive enzymes. It, in conjunction with leptin, also affects neurons in the brain to promote satiety.

Wouldn't stomach acids break up ingested cholecystokinin before it can affect the pancreas and gall bladder? I don't think Satise works for this reason but I could be wrong.

Unless they had a method of delivery to get it past the stomach, you're right, it would just get digested in the stomach as any other protein (it is a protein hormone, by the way).

I haven't looked into literature on CCK in a very very very long time (as in, before leptin and adiponectin were even discovered). My gut reaction is that if it did what they claimed, they wouldn't need to be selling it on an infomercial, although there are often half-truths to these things, so I can look up and see what I find to satisfy your curiousity about a CCK/leptin mechanism. I do know leptin isn't as simple as everyone hoped when they first discovered it either (but isn't that always the case).

Looks like it might work for a very short time, but it's not going to work for long. From a rather long review article on hormones and food intake, here's an excerpt from a section on CCK, with bold emphasis added by me:

Following its release, CCK elicits multiple effects on the gastrointestinal system, including the regulation of gut motility, contraction of the gallbladder, pancreatic enzyme secretion, gastric emptying, and gastric acid secretion.60,61 Most of these are thought to be due to endocrine actions of circulating CCK that has entered the bloodstream. Over 30 years ago, Gibbs et al first demonstrated that exogenous administration of either purified CCK or synthetic CCK-8 into the peritoneal cavity (ip) of rats reduced meal size.62 The response is dose dependent, with larger doses causing a greater reduction of food intake, and they observed that the CCK must be administered near the start of a meal to be effective. If CCK is administered more than 15 minutes before animals begin eating, it has no effect on meal size. The same group also observed that exogenous CCK elicited the same sequence of behaviors that noninjected rats display when they terminate meals.14 Centrally administered CCK also causes animals to consume smaller meals.63,64 The finding that exogenous CCK reduces meal size in rats has been replicated in many labs and extended to numerous species, including nonhuman primates and humans.19,20,65–70

The observation that the administration of exogenous CCK reduces meal size, although consistent with the hypothesis that CCK is a natural satiety factor, is insufficient in and of itself to draw conclusions. Stronger evidence would be the demonstration that endogenous CCK, acting during normal meals, acts to limit caloric intake. Consistent with this, the administration of specific CCK-1 antagonists increases meal size in experimental animals and humans.71–74

Behavioral experiments indicate that CCK is truly a short-term, meal-reducing signal. This is illustrated by the fact that repeated or long-term chronic75 or intermittent76 administration of CCK to rats has no effect on weight loss. When the size of every meal is reduced by CCK, animals compensate by increasing meal frequency.76,77 Although the effects of exogenous CCK are brief, acting within the time of an ongoing meal, CCK also appears to interact with long-term signals of energy balance such as leptin and insulin.78 The anorectic effects of CCK can be augmented by the coadministration of subthreshold concentrations of leptin.79–82 Analogously, administering low doses of insulin directly into the brain also increases the satiating effect of CCK.83,84 Because leptin and insulin are important signals indicating the level of body fat to the brain,1,3,4,85 the implication is that body fat is regulated, at least in part, by changes in the sensitivity to meal-generated satiety signals such as those given by CCK. That is, if an individual loses body weight, the consequently reduced leptin and insulin signals in the brain would render the individual less sensitive to CCK, and there would be a tendency to eat larger meals; the opposite would occur if an individual were to gain body weight. When individuals are chronically obese, however, they are characterized with insulin and leptin resistance; hence, rats with hypothalamic obesity have hyperinsulinemia but a normal sensitivity to CCK’s satiating action,86 and fatty Zucker rats with genetic obesity have slightly reduced sensitivity to CCK.87 Although these forms of obesity are characterized with a blunted response to adiposity hormones, others are characterized by an absent response to CCK. Rats with a spontaneous mutation of the CCK-1 receptor (called OLETF rats88) eat slightly enlarged meals and gradually develop mild obesity over their lifetime.89,90

Thanks Moonbear. I assume "ip" means intra-peritoneal meaning I suspect they injected CCK directly into the abdomen and into the gut. Surely that would be more efficacious then oral means because of the effect of stomach acid on the peptide.

My interest is not diet related, just the biochemistry and my empathy for weight loss endeavours suffered by many.

There are enough diet pills in the world with a host of chemicals that don't belong in your body in large concentrations than they are supposed to be. Whatever happened to good old fashioned exercise and portion control? These people obviously don't realize how good you can feel after a nice jog or swim.

Thanks Moonbear. I assume "ip" means intra-peritoneal meaning I suspect they injected CCK directly into the abdomen and into the gut. Surely that would be more efficacious then oral means because of the effect of stomach acid on the peptide.

Yes, that's intra-peritoneal. The injection doesn't go into the gut, but into the peritoneal cavity. From there, it's pretty rapidly absorbed into circulation. Yes, this would be a more rapid way of getting a drug into circulation than orally. There are ways to get drugs past the stomach to release contents lower in the intestine, but I don't know how this weight-loss pill is manufactured. Frequently, if something needs to get past the stomach, it will be in a capsule form. The capsule dissolves in the mouth or stomach, and then the smaller "beads" inside the capsule are made so they don't dissolve in the stomach, but do in the small intestine when the pH changes and enzymes differ.

misskitty, as long as there are people in the world unwilling to consider exercise and portion control to be a viable means of maintaining their weight-loss, and who remain ignorant about biology, there will be snake-oil salesmen with "quick fix" pills to sell to them.

Frequently, if something needs to get past the stomach, it will be in a capsule form. The capsule dissolves in the mouth or stomach, and then the smaller "beads" inside the capsule are made so they don't dissolve in the stomach, but do in the small intestine when the pH changes and enzymes differ.

Well, thanks for telling me that. Surely then this method is used for this diet pill. That's a satisfactory answer to my question.

Also, I too am very much into health and fitness and advocate such. Wanted to title this "embrace the agony" (of exercising) but though that might offend people with weight problems. You know, exercise is a wonderful catharsis. One-hundred thousand generations gave their lives for our superb physiology. Exercise is a celebration of that lineage!

My earlier comment wasn't intended to be derrogatory. I'm sorry if it was. I'm sorry if I offended anyone in making the comment. It disturbs me that there are people who would take those "quick-fix" pills or try them to see if they work. I just can't see how people can market these drugs to others, knowing they don't work, and still sleep a night. Maybe I'm just too hooked on the energy and that "I worked hard and I LOVE it" feeling I get from therapy (Believe Me! There is a TON of exercise involved with therapy.)